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延迟性脑血管痉挛分子机制研究进展
脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)后严重的并发症之一.其发病率高,治疗棘手,是患者致死或重残的重要原因.SAH后CVS的发生具有时相性.一种为早发性CVS,多发生于SAH后0.5 h至3 d内,常于数小时内缓解.
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动脉瘤性蛛网膜下腔出血后脑血管痉挛的现代诊断和治疗
半个世纪以来,动脉瘤性蛛网膜下腔出血(SAH)引起的脑血管痉挛(cerebral vasospasm,CVS)一直是神经科学领域的研究热点之一,现已部分解决了CVS的诊断、治疗、预防及预后等问题,但依然还存在着不少难以理解及亟待解决的问题.
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Objective To undertake animal experimentation and clinical study on the safety and efficacy of percutaneous transluminal angioplasty (PTA) and intraarterial papaverine (IAP) infusion for treatment of refractory symptomatic cerebral vasospasm (CVS). Methods In the experimental study, vasospasm was induced in rabbits by double injections of blood into the cisterna magna, IAP infusion was given on either the 4th day or the 7th day after occurrence of subarachnoid hemorrhage (SAH), and then neurological observation, angiography, light and electron microscopy were done. In the clinical study, since September 1996, 22 patients with refractory symptomatic CVS involving 50 vascular territories received dilation therapy by PTA and IAP within 24 hours of clinical neurological deterioration. Results In the experimental study, all the rabbits except two in the 'the 4th day' group showed angiographic dilation in all of the spastic basilar arteries, and neurological improvement; in the ' the 7th day' group angiographic dilation appeared in 4 (57. 1% ) out of 7 rabbits. After 24 hours, 1 rabbit in each group had recurrence of neurological deficits and angiographic constriction. In the clinical study after aneurysm clipping or endovascular coil embolization was done, within 72 hours of SAH all patients underwent endovascular treatment: PTA alone in 3 cases, IAP alone in 14 cases, PTA and IAP in the remaining 5 cases. All vessel segments were dilated satisfactorily after endovascular treatment. Clinical improvement was significant in 13 cases,moderate in 7, minimal or none in 2; 2 cases died on the 7th day after endovascular dilation treatment. Conclusion Endovascular dilating techniques, namely, PTA, IAP and a combination of PTA and IAP, are safe and effective for treatment of symptomatic CVS refractory to medical therapy.
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颅脑创伤后脑血管痉挛的诊断及治疗体会
颅脑外伤后许多患者有病情逐渐加重过程,部分患者甚至死亡.如果排除非颅内因素(即全身原因),病情加重多与颅内血肿增大、迟发性颅内血肿或脑水肿加重等有关,头颅CT检查常能发现其病因.但部分患者病情加重不能用颅脑CT检查结果解释,可能与症状性脑血管痉挛( symptomatic cerebral vasospasm,SCVS)有关,本院自2006年6月至2009年6月收治相关病例26例,现报告如下.资料与方法1.一般资料:本组颅脑外伤26例,男18例,女8例,年龄22~72岁,平均43.3岁;车祸伤17例,高处坠落伤7例,打击伤2例;合并高血压8例,糖尿病3例.
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蛛网膜下腔出血后脑血管痉挛40例分析
蛛网膜下腔出血(Subarachnoid hemorrhage,SAH)后脑血管痉挛,为脑底大动脉的一支或多支由于动脉壁平滑肌的收缩或血管损伤引起其管壁狭窄[1].根据痉挛发生时间可分为急性痉挛,发生在SAH后的短时间内;迟发性痉挛(Delayed cerebral vasospasm,DCVS),发生在SAH后几天或几周者[2].我院1990年以来收住的108例SAH患者中,有40例(占37.0%)发生DCVS,报道如下.
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一种新的兔株网膜下腔出血后症状性脑血管痉挛模型的建立
Objective To establish an experimental model of symptomatic cerebral vasospasm(CVS) after subarachnoid hemorrhage( SAH) in rabbits. Method 2 weeks after the ligation of bilateral common carotid arteries, We induced CVS by injecting arterial blood twice via a cranial hole 2 mm× 2 mm and then neurological symptoms ,cerebral blood flow(rCBF) and food intake were evaluated. Results Food intake and rCBF decreased and neurological disorders were observed. Conclusion An experimental rabbit model of symptomatic CVS can be established by injecting blood via a cranial hole after bilateral common carotid arteries ligation. ``
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蛛网膜下腔出血并发脑血管痉挛预防的实验与临床研究进展
Cerebral vasospasm(CVS),a common complication of subarachnoid hemorrhage(SAH),is caused by many factors and associated with poor prognosis of SAH.CVS generally occurs 3-4 days after the initial SAH and peaks at 5-7 days.
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24例蛛网膜下腔出血后迟发性脑血管痉挛临床分析
蛛网膜下腔出血(Subarachnoid hemorrhage,SAH)后脑血管痉挛为脑底大动脉的一支或多支由于动脉壁平滑肌的收缩或血管损伤引起其管腔狭窄.根据痉挛发生的时间可分为急性和迟发性,急性脑血管痉挛在SAH后立即出现,持续时间短,多在数10 min或数小时缓解;迟发性脑血管痉挛(Delayed cerebral vasospasm,DCDV)发生在SAH后3~4 d,第2周达高峰,一般需3周左右的恢复过程.
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实验性蛛网膜下腔出血基底动脉的形态学干预研究
自发性蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后脑血管痉挛的实验研究已经表明,动脉血管壁的形态学改变在脑血管痉挛的(cerebral vasospasm,CVS)病因中具有非常重要的作用,早期研究是认为肌层的病理学改变对CVS发生具有重要促进作用.但是近期实验研究发现SAH后脑血管痉挛存在内皮细胞和平滑肌细胞的凋亡及血管壁细胞的增殖的现象.本研究对SD大鼠SAH后基底动脉进行形态学变化的数值测定及组织病理学观察,动态展示了SAH后CVS的如何发生、怎样发展、终演变的过程;通过对SD大鼠SAH后脑基底动脉电镜下超微结构的观察研究,从超微角度探讨了SAH后迟发脑血管痉挛(delayed cerebral vasospasm,DCVS)的发生机制,本文以细胞凋亡水平作为研究的出发点,丰富SAH后CVS的分子生物学机制,同时还探讨了环孢素(CsA)抗细胞凋亡在治疗大鼠蛛网膜下腔出血后脑血管痉挛的作用.
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蛛网膜下腔出血致脑血管痉挛诊治分析
脑血管痉挛(Cerebral vasospasm,CVS)是蛛网膜下腔出血(Subarachnoid hemorrhage,SAH)后致死或致残的主要原因,SAH后CVS,为脑底大动脉的一支或多支由于动脉壁平滑肌的收缩或血管损伤引起其管腔狭窄[1].